Human immunopathogenesis of severe acute respiratory syndrome (SARS)
Identifieur interne : 003688 ( Main/Exploration ); précédent : 003687; suivant : 003689Human immunopathogenesis of severe acute respiratory syndrome (SARS)
Auteurs : Mark J. Cameron [Canada] ; Jesus F. Bermejo-Martin [Espagne] ; Ali Danesh [Canada] ; Matthew P. Muller [Canada] ; David J. Kelvin [Canada]Source :
- Virus Research [ 0168-1702 ] ; 2007.
Descripteurs français
- KwdFr :
- Cytokines (immunologie), Cytokines (métabolisme), Humains, Immunité innée, Interactions hôte-pathogène, Modèles biologiques, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (génétique), Syndrome respiratoire aigu sévère (immunologie), Séquençage par oligonucléotides en batterie, Virus du SRAS (immunologie).
- MESH :
- anatomopathologie : Syndrome respiratoire aigu sévère.
- génétique : Syndrome respiratoire aigu sévère.
- immunologie : Cytokines, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : Cytokines.
- Humains, Immunité innée, Interactions hôte-pathogène, Modèles biologiques, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- Cytokines (immunology), Cytokines (metabolism), Host-Pathogen Interactions, Humans, Immunity, Innate, Models, Biological, Oligonucleotide Array Sequence Analysis, SARS Virus (immunology), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology).
- MESH :
- chemical , immunology : Cytokines.
- chemical , metabolism : Cytokines.
- genetics : Severe Acute Respiratory Syndrome.
- immunology : SARS Virus, Severe Acute Respiratory Syndrome.
- pathology : Severe Acute Respiratory Syndrome.
- Host-Pathogen Interactions, Humans, Immunity, Innate, Models, Biological, Oligonucleotide Array Sequence Analysis.
Abstract
Progressive immune-associated injury is a hallmark of severe acute respiratory syndrome (SARS). Viral evasion of innate immunity, hypercytokinemia and systemic immunopathology in the SARS coronavirus (SARS CoV) infected host have been suggested as possible mechanisms for the cause of severe pathology and morbidity in SARS patients. The molecular and cellular basis for how SARS CoV impacts the host immune system resulting in severe SARS, however, has not been elucidated. The variable clinical course of SARS may be the result of complex programs of host responses against the infectious agent. Therefore, the systematic analysis of innate and adaptive immune responses to SARS CoV is imperative in building as complete an immunological model as possible of host immunity and inflammatory responses during illness. Here we review recent advances in SARS immunopathogenesis research and present a summary of our findings regarding host responses in SARS patients. We contend that dysregulated type I and II interferon (IFN) responses during SARS may culminate in a failure of the switch from hyper-innate immunity to protective adaptive immune responses in the human host.
Url:
DOI: 10.1016/j.virusres.2007.02.014
PubMed: 17374415
PubMed Central: 7114310
Affiliations:
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Le document en format XML
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Muller</name><affiliation wicri:level="4"><nlm:aff id="aff2">University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="aff4">Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5</wicri:regionArea><wicri:noRegion>Ontario M5G 1X5</wicri:noRegion></affiliation></author><author><name sortKey="Kelvin, David J" sort="Kelvin, David J" uniqKey="Kelvin D" first="David J." last="Kelvin">David J. Kelvin</name><affiliation wicri:level="1"><nlm:aff id="aff1">University Health Network, MaRS Centre, 101 College Street, Toronto, Ontario M5G 1L7, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University Health Network, MaRS Centre, 101 College Street, Toronto, Ontario M5G 1L7</wicri:regionArea><wicri:noRegion>Ontario M5G 1L7</wicri:noRegion></affiliation><affiliation wicri:level="4"><nlm:aff id="aff2">University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation></author></analytic><series><title level="j">Virus Research</title><idno type="ISSN">0168-1702</idno><idno type="eISSN">1872-7492</idno><imprint><date when="2007">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cytokines (immunology)</term><term>Cytokines (metabolism)</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>Immunity, Innate</term><term>Models, Biological</term><term>Oligonucleotide Array Sequence Analysis</term><term>SARS Virus (immunology)</term><term>Severe Acute Respiratory Syndrome (genetics)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Severe Acute Respiratory Syndrome (pathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cytokines (immunologie)</term><term>Cytokines (métabolisme)</term><term>Humains</term><term>Immunité innée</term><term>Interactions hôte-pathogène</term><term>Modèles biologiques</term><term>Syndrome respiratoire aigu sévère (anatomopathologie)</term><term>Syndrome respiratoire aigu sévère (génétique)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Séquençage par oligonucléotides en batterie</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cytokines</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Host-Pathogen Interactions</term><term>Humans</term><term>Immunity, Innate</term><term>Models, Biological</term><term>Oligonucleotide Array Sequence Analysis</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Immunité innée</term><term>Interactions hôte-pathogène</term><term>Modèles biologiques</term><term>Séquençage par oligonucléotides en batterie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Progressive immune-associated injury is a hallmark of severe acute respiratory syndrome (SARS). Viral evasion of innate immunity, hypercytokinemia and systemic immunopathology in the SARS coronavirus (SARS CoV) infected host have been suggested as possible mechanisms for the cause of severe pathology and morbidity in SARS patients. The molecular and cellular basis for how SARS CoV impacts the host immune system resulting in severe SARS, however, has not been elucidated. The variable clinical course of SARS may be the result of complex programs of host responses against the infectious agent. Therefore, the systematic analysis of innate and adaptive immune responses to SARS CoV is imperative in building as complete an immunological model as possible of host immunity and inflammatory responses during illness. Here we review recent advances in SARS immunopathogenesis research and present a summary of our findings regarding host responses in SARS patients. We contend that dysregulated type I and II interferon (IFN) responses during SARS may culminate in a failure of the switch from hyper-innate immunity to protective adaptive immune responses in the human host.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Antonio, G E" uniqKey="Antonio G">G.E. Antonio</name></author><author><name sortKey="Ooi, C G" uniqKey="Ooi C">C.G. Ooi</name></author><author><name sortKey="Wong, K T" uniqKey="Wong K">K.T. Wong</name></author><author><name sortKey="Tsui, E L" uniqKey="Tsui E">E.L. Tsui</name></author><author><name sortKey="Wong, J S" uniqKey="Wong J">J.S. Wong</name></author><author><name sortKey="Sy, A N" uniqKey="Sy A">A.N. Sy</name></author><author><name sortKey="Hui, J Y" uniqKey="Hui J">J.Y. Hui</name></author><author><name sortKey="Chan, C Y" uniqKey="Chan C">C.Y. Chan</name></author><author><name sortKey="Huang, H Y" uniqKey="Huang H">H.Y. 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Julkunen</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Canada</li><li>Espagne</li></country><region><li>Castille-et-León</li><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><country name="Canada"><noRegion><name sortKey="Cameron, Mark J" sort="Cameron, Mark J" uniqKey="Cameron M" first="Mark J." last="Cameron">Mark J. Cameron</name></noRegion><name sortKey="Cameron, Mark J" sort="Cameron, Mark J" uniqKey="Cameron M" first="Mark J." last="Cameron">Mark J. Cameron</name><name sortKey="Danesh, Ali" sort="Danesh, Ali" uniqKey="Danesh A" first="Ali" last="Danesh">Ali Danesh</name><name sortKey="Danesh, Ali" sort="Danesh, Ali" uniqKey="Danesh A" first="Ali" last="Danesh">Ali Danesh</name><name sortKey="Kelvin, David J" sort="Kelvin, David J" uniqKey="Kelvin D" first="David J." last="Kelvin">David J. Kelvin</name><name sortKey="Kelvin, David J" sort="Kelvin, David J" uniqKey="Kelvin D" first="David J." last="Kelvin">David J. Kelvin</name><name sortKey="Muller, Matthew P" sort="Muller, Matthew P" uniqKey="Muller M" first="Matthew P." last="Muller">Matthew P. Muller</name><name sortKey="Muller, Matthew P" sort="Muller, Matthew P" uniqKey="Muller M" first="Matthew P." last="Muller">Matthew P. Muller</name></country><country name="Espagne"><region name="Castille-et-León"><name sortKey="Bermejo Martin, Jesus F" sort="Bermejo Martin, Jesus F" uniqKey="Bermejo Martin J" first="Jesus F." last="Bermejo-Martin">Jesus F. Bermejo-Martin</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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